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Dietary fat intake, pesticide use, and Parkinson's disease.
Parkinsonism Relat Disord. 2014 Jan; 20(1):82-7.PR

Abstract

BACKGROUND

Dietary fat intake may modify Parkinson's disease (PD) risk directly or by altering the response to environmental neurotoxicants including pesticides.

METHODS

We conducted a case-control study of PD nested in the Agricultural Health Study (AHS), a cohort of pesticide applicators and spouses. We evaluated diet and pesticide use before diagnosis in 89 PD cases, confirmed by movement disorder specialists, or a corresponding date in 336 frequency-matched controls. Associations were evaluated using multivariate logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs).

RESULTS

In the AHS, PD was inversely associated with N-3 polyunsaturated fatty acids (PUFAs) (OR 0.4, 95% CI 0.2-0.8 for highest vs. lowest tertile) and the N-3 precursor α-linolenic acid (0.4, 0.2-0.8). In a meta-analysis of nine studies, including the present one, PD was inversely associated with α-linolenic acid (0.81, 0.68-0.96). In the AHS, associations of PD with the pesticides paraquat and rotenone were modified by fat intake. The OR for paraquat was 4.2 (1.5-12) in individuals with PUFA intake below the median but 1.2 (0.4-3.4) in those with higher intake (p-interaction = 0.10). The OR for rotenone was 5.8 (2.3-15) in those with saturated fat intake above the median but 1.5 (0.5-4.2) in those with lower intake (p-interaction = 0.02).

CONCLUSIONS

PUFA intake was consistently associated with lower PD risk, and dietary fats modified the association of PD risk with pesticide exposure. If confirmed, these findings suggest that a diet high in PUFAs and low in saturated fats might reduce risk of PD.

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Authors+Show Affiliations

Kamel F
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA. Electronic address: kamel@niehs.nih.gov.
Goldman SM
The Parkinson's Institute, Sunnyvale, CA, USA.
Umbach DM
Biostatistics Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA.
Chen H
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.
Richardson G
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.
Barber MR
Westat Inc, Durham, NC, USA.
Meng C
The Parkinson's Institute, Sunnyvale, CA, USA.
Marras C
Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada.
Korell M
The Parkinson's Institute, Sunnyvale, CA, USA.
Kasten M
Department of Neurology, University of Lübeck, Lübeck, Germany; Department of Clinical and Molecular Neurogenetics, University of Lübeck, Lübeck, Germany.
Hoppin JA
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.
Comyns K
The Parkinson's Institute, Sunnyvale, CA, USA.
Chade A
Institute of Cognitive Neurology, Institute of Neuroscience, Favaloro University, Buenos Aires, Argentina.
Blair A
Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD, USA.
Bhudhikanok GS
The Parkinson's Institute, Sunnyvale, CA, USA.
Webster Ross G
Veterans Affairs Pacific Islands Health Care System, Honolulu, HI, USA.
William Langston J
The Parkinson's Institute, Sunnyvale, CA, USA.
Sandler DP
Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, NC, USA.
Tanner CM
The Parkinson's Institute, Sunnyvale, CA, USA.

MeSH

AdultAgedAged, 80 and overCase-Control StudiesDietDietary FatsFatty Acids, Omega-3FemaleHumansMaleMiddle AgedParkinson DiseasePesticidesRisk Factors

Pub Type(s)

Journal Article
Meta-Analysis
Research Support, N.I.H., Extramural
Research Support, N.I.H., Intramural

Language

eng

PubMed ID

24120951

Citation

Kamel, Freya, et al. "Dietary Fat Intake, Pesticide Use, and Parkinson's Disease." Parkinsonism & Related Disorders, vol. 20, no. 1, 2014, pp. 82-7.
Kamel F, Goldman SM, Umbach DM, et al. Dietary fat intake, pesticide use, and Parkinson's disease. Parkinsonism Relat Disord. 2014;20(1):82-7.
Kamel, F., Goldman, S. M., Umbach, D. M., Chen, H., Richardson, G., Barber, M. R., Meng, C., Marras, C., Korell, M., Kasten, M., Hoppin, J. A., Comyns, K., Chade, A., Blair, A., Bhudhikanok, G. S., Webster Ross, G., William Langston, J., Sandler, D. P., & Tanner, C. M. (2014). Dietary fat intake, pesticide use, and Parkinson's disease. Parkinsonism & Related Disorders, 20(1), 82-7. https://doi.org/10.1016/j.parkreldis.2013.09.023
Kamel F, et al. Dietary Fat Intake, Pesticide Use, and Parkinson's Disease. Parkinsonism Relat Disord. 2014;20(1):82-7. PubMed PMID: 24120951.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary fat intake, pesticide use, and Parkinson's disease. AU - Kamel,Freya, AU - Goldman,Samuel M, AU - Umbach,David M, AU - Chen,Honglei, AU - Richardson,Gina, AU - Barber,Marie Richards, AU - Meng,Cheryl, AU - Marras,Connie, AU - Korell,Monica, AU - Kasten,Meike, AU - Hoppin,Jane A, AU - Comyns,Kathleen, AU - Chade,Anabel, AU - Blair,Aaron, AU - Bhudhikanok,Grace S, AU - Webster Ross,G, AU - William Langston,J, AU - Sandler,Dale P, AU - Tanner,Caroline M, Y1 - 2013/10/01/ PY - 2013/06/17/received PY - 2013/09/10/revised PY - 2013/09/23/accepted PY - 2013/10/15/entrez PY - 2013/10/15/pubmed PY - 2014/9/13/medline KW - Dietary fat KW - Parkinson's disease KW - Pesticides KW - Polyunsaturated fatty acids SP - 82 EP - 7 JF - Parkinsonism & related disorders JO - Parkinsonism Relat Disord VL - 20 IS - 1 N2 - BACKGROUND: Dietary fat intake may modify Parkinson's disease (PD) risk directly or by altering the response to environmental neurotoxicants including pesticides. METHODS: We conducted a case-control study of PD nested in the Agricultural Health Study (AHS), a cohort of pesticide applicators and spouses. We evaluated diet and pesticide use before diagnosis in 89 PD cases, confirmed by movement disorder specialists, or a corresponding date in 336 frequency-matched controls. Associations were evaluated using multivariate logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: In the AHS, PD was inversely associated with N-3 polyunsaturated fatty acids (PUFAs) (OR 0.4, 95% CI 0.2-0.8 for highest vs. lowest tertile) and the N-3 precursor α-linolenic acid (0.4, 0.2-0.8). In a meta-analysis of nine studies, including the present one, PD was inversely associated with α-linolenic acid (0.81, 0.68-0.96). In the AHS, associations of PD with the pesticides paraquat and rotenone were modified by fat intake. The OR for paraquat was 4.2 (1.5-12) in individuals with PUFA intake below the median but 1.2 (0.4-3.4) in those with higher intake (p-interaction = 0.10). The OR for rotenone was 5.8 (2.3-15) in those with saturated fat intake above the median but 1.5 (0.5-4.2) in those with lower intake (p-interaction = 0.02). CONCLUSIONS: PUFA intake was consistently associated with lower PD risk, and dietary fats modified the association of PD risk with pesticide exposure. If confirmed, these findings suggest that a diet high in PUFAs and low in saturated fats might reduce risk of PD. SN - 1873-5126 UR - https://www.unboundmedicine.com/medline/citation/24120951/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S1353-8020(13)00353-2 DB - PRIME DP - Unbound Medicine ER -